IMR Press / FBS / Volume 3 / Issue 2 / DOI: 10.2741/S170

Frontiers in Bioscience-Scholar (FBS) is published by IMR Press from Volume 13 Issue 1 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Protective mechanisms by cystatin C in neurodegenerative diseases
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1 Nathan S. Kline Institute, Orangeburg, NY, 10962, U.S.A.
2 Departments of Psychiatry and Pharmacology, New York University School of Medicine, New York, NY, 10016, U.S.A.

*Author to whom correspondence should be addressed.

Academic Editor: Roberta Ghidoni

Front. Biosci. (Schol Ed) 2011, 3(2), 541–554;
Published: 1 January 2011

Neurodegeneration occurs in acute pathological conditions such as stroke, ischemia, and head trauma and in chronic disorders such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. While the cause of neuronal death is different and not always known in these varied conditions, hindrance of cell death would be beneficial in the prevention of, slowing of, or halting disease progression. Enhanced cystatin C (CysC) expression in these conditions caused a debate as to whether CysC up-regulation facilitates neurodegeneration or it is an endogenous neuroprotective attempt to prevent the progression of the pathology. However, recent in vitro and in vivo data have demonstrated that CysC plays protective roles via pathways that are dependent on inhibition of cysteine proteases, such as cathepsin B, or by induction of autophagy, induction of proliferation, and inhibition of amyloid-beta aggregation. Here we review the data demonstrating the protective roles of CysC under conditions of neuronal challenge and the protective pathways induced under various conditions. These data suggest that CysC is a therapeutic candidate that can potentially prevent brain damage and neurodegeneration.

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